Pathophysiology Review Questions – 1

Front 1

1. What are the functions of ribosomes, lysosomes, mitochondria, smooth and rough endoplasmic reticulum, and Golgi apparatus?

Back 1

ribosomes---cell structures that utilize mRNA to make protiens
lysosomes---cell sructures that contain digestive enzymes to break down other materials
mitochondria---cellular structure that produces ATP for energy
smooth and rough endoplasmic reticulum---have no ribosomes attached
golgi apparatus---processes and packages macromolecules synthesized by the cell

Front 2

2. What are the functions of the plasma membrane proteins?

Back 2

transport, enzyme, cell surface receptor, cell surface markers, cell adhesion, atachment of cell cytoskeleton

Front 3

3. Why can’t glucose, amino acids, sodium and calcium ions move across the cell membrane?

Back 3

they require another substance (hormone, enzyme, etc) to facilitate tgheir crossing the cell membrane

Front 4

4. What are the differences among uniport, symport, and antiport?

Back 4

uniport---one direction movement
symport---2 molecules moving simultaneoulsy in one direction
antiport---opposite directions

Front 5

5. What are the functions of endocytosis and exocytosis?

Back 5

exocytosis--- is when cells active transport mechanisms by which the cells move large protiens--secrete substances such as hormones and neurotransmitters

Front 6

6. Define atrophy, hypertrophy, hyperplasia, metaplasia, and dysplasia.
p.46

Back 6

atrrophy---decrease in cell size
hypertrophy---cells and organs increase due to increase of protein
hyperplasia---increase in the number of cells due to increased rate of cellular division
metaplasia---reversablecell process wherein tissues change beyond normal cell growth
dysplasia---

Front 7

7. List general mechanisms of cell injury.

Back 7

hypoxic injury-lack of sufficient oxygen
free radicals-electrically uncharged atom or group of atoms having an unpaired electron which makes it unstable
chemical injury---biochemical interaction between a toxic substance and the cell's plasma membrane
physical---
biological---
other---immunologic and inflammitory, genetic, nutritional

Front 8

8. What are the reversible and irreversible changes of hypoxic injury?

Back 8

reversable---ATP depletion, cell swelling, detachment of ribosomes
irriversable---point of no return, severe vauolization occurs of the mitochondria and Ca++ moves into the cell.....loss of phospholipids, changes in cytoskeleton, inflammation, free radicals flare, lipid breakdown

Front 9

9. How does ionizing radiation cause cell damage?

Back 9

direct damage to DNA, free radicals damage DNA

Front 10

10. What is the difference between necrosis and apoptosis?

Back 10

apoptosis--- is programed cell death
necrosis---sum of cellular changes after local cell death and the process of cellular autodigestion

Front 11

11. What are the common locations of coagulative, liquefactive, caseous, fat, and gangrenous necrosis?

Back 11

necrosis:
coagulative---Ht Kd, adrenal glands
liquefactive---Neurons and glial cells of the brain,
Hydrolytic enzymes
caseous---Tuberculous pulmonary infection
Combination of coagulative and liquefactive necrosis
fat---Breast, pancreas, and other abdominal organs
Action of lipases
gangrenous---limbs, toes fingers...Clinical term
Dry vs. wet gangrene
Gas gangrene

Front 12

12. What are the mechanisms of edema?

Back 12

increased capillary permeability and hydrostatic pressure and lymph obstruction

Front 13

13. How are thirst and ADH secretion regulated?

Back 13

increased thirst and then ADH is released

Front 14

14. How are acidosis and alkalosis compensated?

Back 14

acidosis ---is hyperventilaiton and increased acid titration
alkalosis---is hypo and decreased acid titration

Front 15

15. Describe the flow of the genetic information in the cell.

Back 15

DNA replicaition, RNA transcription, RNA translation

Front 16

16. What are the karyotypes of Down, Turner, and Klinefelter syndromes?

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down syndrome----trisomy 21
kleinfleter---XXY or XXXY for a boy
turner---a girl with only 1 X chromosome

Front 17

17. Describe the effects of genes and environment on the development of disease.

Back 17

genetic orgin---cystic fibrosis
environmental-pneumonia
genetic and environment---diabetes

Front 18

18. List 10 examples of adult multifactorial diseases.

Back 18

coronary heart disease
hypertension
breast cancer
colorectal cancer
diabetes
obesity
alhemers
alcohoism
psciatric disorders
NOT---Amoyotrophic Lateral Sclerosis

Front 19

19. What are the 3 lines of body defenses?

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-First line of defense
Innate resistance
-Second line of defense
Inflammation
-Third line of defense
Adaptive (acquired) immunity

Front 20

20. What are the local manifestations of inflammation?

Back 20

Redness
Swelling
Pain
Loss of function

.....Acute Inflammatory ResponseCauses
Infection, mechanical damage, ischemia, nutrient deprivation, temperature extremes, radiation, etc.
Vascular responses
Blood vessel dilation, increased vascular permeability and leakage, white blood cell adherence to the inner walls of the vessels and migration through the vessels
----

Front 21

21. What are the systemic effects of inflammation?

Back 21

-Fever
-Leukocytosis
-Increased levels of circulating plasma proteins

Front 22

22. What cells are involved in chronic inflammation?

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Inflammation lasts 2 weeks or longer
May occur as a distinct process without much acute inflammation
Characterized by a ......

-dense infiltration of lymphocytes and macrophages (developed from circulatory monocytes)
<If macrophages are unable to protect the host from tissue damage, the body attempts to wall off and isolate the infected site, thus forming a granuloma>

Front 23

23. What are the features of acquired (adaptive) immunity?

Back 23

specifity, memory function, antibody/antigen and lymphocyte activity

Front 24

24. What cells produce antibodies?

Back 24

plasma cells

Front 25

25.Define allergy, autoimmunity, and alloimmunity

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*hypersensitivity:Altered immunologic response to an antigen that results in disease or damage to the host
Allergy---Deleterious effects of hypersensitivity to environmental (exogenous) antigens
Autoimmunity---Disturbance in the immunologic tolerance of self-antigens
Alloimmunity---Immune reaction to tissues of another individual

Front 26

26. What are the characteristics and examples of 4 types of hypersensitivities?

Back 26

Characterized by the immune mechanism.....
1. Type I (anaphylactic) IgE mediated. For example, hay fever, penicillin shock

2. Type II (cytotoxic)
Tissue-specific reactions
For example, incompatible blood transfusion, Graves disease

3.Type III (immune complex)
Antigen-antibody-complement activation. For example, glomerulonephritis, rheumatoid arthritis

4.Type IV (delayed)
Cell mediated. For example, contact dermatitis, graft rejection, poisen ivy

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27. What are the 4 sequential stages of infection?

Back 27

Colonization---Pathogens present on or in the body without tissue invasion

Invasion---Resists host defenses by attaching to host cells

Multiplication---Uses host nutrients and environment for reproduction

Spread---Migrates locally or through bloodstream and lymphatics

Front 28

28. What is the number one cause of death worldwide?

Back 28

infectious disease

Front 29

29. What body systems are involved in stress response?

Back 29

nervous, endocrine, immune

Front 30

30. What are the 3 successive stages of general adaptation syndrome?

Back 30

Alarm stage
CNS is aroused and body’s defenses are mobilized
Stage of resistance or adaptation
Mobilization contributes to fight or flight responses
Stage of exhaustion
Continuous stress causes progressive breakdown of compensatory mechanisms
alarm---CNS is aware of body's defense
adaption---flight or fright
exhaustion---homeostasis

Front 31

31. List common stress-related diseases and conditions.

Back 31

---Cardiovascular system: CAD, hypertension, stroke, and arrhythmias
---Muscular system: tension headache, and muscle contraction backache
---Connective tissues: RA, and other autoimmune diseases
---Pulmonary system: asthma, and hay fever
---Immune system: immunodeficiency or suppression, and autoimmune diseases
---Gastrointestinal system: ulcer, IBS, diarrhea, nausea and vomiting, and ulcerative colitis
----Genitourinary system: diuresis, impotence, and frigidity
---Integumentary system: eczema, neurodermatitis, and acne
---Endocrine system: diabetes mellitus, and amenorrhea
---Central nervous system: fatigue and lethargy, type A behavior, overeating, depression, and insomnia

Front 32

32. What is cancer?

Back 32

abnormal growth, division and cell differentiation

Front 33

33. How do benign tumors differentiated from malignant tumors?

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benign is encapsulated..similar to normal cells

malignant---rapid growth, invasive, nonincapsulated,not differentiated, high mitotic index, can spread distantly

Front 34

34.What are the characteristics of cancer?

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Transformation
The process by which a normal cell becomes a cancer cell
Autonomy
Cancer cell’s independence from normal cellular controls
Anaplasia
Loss of differentiation, which is the process of developing specialized functions

Front 35

35. How is cancer graded?

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The higher the grade, the more aggressive the cancer

Front 36

36. How does cancer spread? Describe how breast cancer metastasizes.

Back 36

Dysplasia
Disorderly but non-cancerous growth and reversible change, featured by pleomorphism (wide variation in the shape and size of cells and nuclei), hyperchromatism (darkly stained nuclei), and loss of normal orientation
In situ neoplasm: cancer in the original location
Invasive neoplasm: cancer in deeper tissues

Front 37

Describe the TNM system of cancer staging.

Back 37

Based on the anatomic extent of the tumor, including the size of the primary tumor, the degree to which it has invaded, and the extent to which it has spread
The higher the stage, the larger, more invasive and metastatic the tumor
Stages
Stage 1: confined to its organ of origin
Stage 2: locally invasive
Stage 3: regional structures
Stage 4: distant sites

Front 38

38. What are the common clinical manifestations of cancer?

Back 38

Syndrome of cachexia.Most severe form of malnutrition. Present in 80% of cancer patients at death. Manifested by:

Anorexia- early satiety, weight loss, anemia, asthenia, taste alterations, and altered protein, lipid, and carbohydrate metabolism

Anemia-A decrease of hemoglobin in the blood
Mechanisms

Chronic bleeding- resulting in iron deficiency, severe malnutrition, medical therapies, or malignancy in blood-forming organs

-Leukopenia and thrombocytopenia-
Direct tumor invasion to the bone marrow causes both leukopenia and thrombocytopenia.....
Chemotherapy drugs are toxic to the bone marrow

Infection-Risk increases when the absolute neutrophil and lymphocyte counts fall
Paraneoplastic syndromes
Symptom complexes that cannot be explained by the local or distant spread of the tumor or by the effects of hormones released by the tissue from which the tumor arose

Front 39

39. What are the 3 leading causes of death in children?

Back 39

leukemias, CNS tumors, sarcomas, and embryonic tumors

Front 40

40. What are the common childhood cancers? test

Back 40

Retinoblastoma
Neuroblastoma
Nephroblastoma